2018
DOI: 10.1128/jvi.00672-18
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The Human T-Cell Leukemia Virus Type 1 Basic Leucine Zipper Factor Attenuates Repair of Double-Stranded DNA Breaks via Nonhomologous End Joining

Abstract: Adult T-cell leukemia (ATL) is a fatal malignancy of CD4 T cells infected with human T-cell leukemia virus type 1 (HTLV-1). ATL cells often exhibit random gross chromosomal rearrangements that are associated with the induction and improper repair of double-stranded DNA breaks (DSBs). The viral oncoprotein Tax has been reported to impair DSB repair but has not been shown to be consistently expressed throughout all phases of infection. The viral oncoprotein HTLV-1 basic leucine zipper (bZIP) factor (HBZ) is cons… Show more

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Cited by 18 publications
(17 citation statements)
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“…Indeed, the bZIP domain of HBZ was previously found to interact with MafG in vitro [67]. Moreover, we have used a proteomic approach to identify cellular proteins that interact with HBZ, and from this analysis, all three small Mafs arose as potential HBZ-binding partners (Fig 4A)[68]. The small Maf peptides identified are shown in S4 Fig.…”
Section: Resultsmentioning
confidence: 98%
“…Indeed, the bZIP domain of HBZ was previously found to interact with MafG in vitro [67]. Moreover, we have used a proteomic approach to identify cellular proteins that interact with HBZ, and from this analysis, all three small Mafs arose as potential HBZ-binding partners (Fig 4A)[68]. The small Maf peptides identified are shown in S4 Fig.…”
Section: Resultsmentioning
confidence: 98%
“…Integration could also be enhanced by attenuating double-strand break repair ( Fig. 5 ), similar to the repression of HR and base excision repair by human T-lymphotropic virus 1 (HTLV-1), to facilitate viral integration ( 84 86 ). Moreover, the induction of DNA breaks ( Fig.…”
Section: Discussionmentioning
confidence: 99%
“…However, multidrug resistance and treatment are key factors in the failure of leukemia treatment. Several factors are involved in the mechanism of leukemia resistance, including ABC transporter-mediated multidrug resistance [17], DNA repair abnormalities [18], variations in the bone marrow microenvironment [19], and abnormal expression of noncoding RNAs including circRNA, miRNA, and LncRNA [20]. Undeniably, ncRNAs have opened up new prospects for AML diagnosis, prognosis, and treatment.…”
Section: Discussionmentioning
confidence: 99%